Clinical & Experimental Cardiology
Open Access

A Brief Description on Pathophysiology of Ischemic Stroke

Xianwu Cheng^{* *}Correspondence: Xianwu Cheng, Department of Anesthesiology, Yanbian University Hospital, Yanji, China, Email:

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Description

Ischemic stroke caused by obstruction of a cerebral artery is one of the leading causes of chronic impairment globally, and there are still few effective ways to promote functional recovery after a cerebral stroke. A severe lack of blood supply to the brain after an ischemic stroke results in insufficient oxygen supply to the brain, which leads to neuronal death. Ischemic tissue injury is caused by inflammatory responses at the blood-endothelial interface of brain capillaries. Inflammatory interactions at the blood-endothelial interface, such as adhesion molecules, cytokines, chemokine’s, and white blood cells, are also important in the pathogenesis of tissue injury in cerebral infarction. Ion imbalance, neuro-inflammation, and aberrant immune cell activation are all pathophysiological alterations that can lead to neuronal death after an ischemic stroke.

However, despite substantial investigation, the specific processes of stroke injury remain unknown. It is undeniable that ILs has a significant role in the course of ischemic stroke. A lymphocyte medium that interacts between white blood cells or immune cells is referred to as IL. It belongs to the same cytokine family as blood cell growth factor. Both IL and hemolytic growth factor are cytokines that work together to complete hematopoiesis and immune regulatory activities. IL is involved in the transmission of information, the activation and regulation of immune cells, as well as the activation, multiplication, and differentiation of T cells and B cells, as well as the inflammatory response.

The pathophysiology of ischemic stroke is closely linked to interleukin (IL). This study will look at the role of IL in the pathophysiology of stroke, the relationships between distinct ILmediated pathways, the impact of different mediators on different cell types, and how different ILs govern complicated inflammatory cascades.

Mechanism of pleiotropic effects of IL-1

IL-1 is a multifunctional cytokine that has a wide range of biological effects in a variety of cell types, many of which are linked to stroke risk and outcome. Increased expression of cytokines, chemokine’s, and growth factors, activation of matrix metalloproteinase, up regulation of adhesion molecules, increased leukocyte infiltration, activation of platelets, blood flow changes, increased angiogenesis, decreased neurogenesis, and numerous other effects are all downstream effects of IL-1.

Increased systemic inflammation, which is mediated in part by IL-1, is linked to stroke-related comorbidities and risk factors.

In the acute phase after a stroke, an increase in IL-1 in the brain mediates the harmful inflammatory process, which includes upregulation of IL-6, TNF-, MMP-9, and chemokine’s in astrocytes; inhibition of neurogenesis; increase of adhesion molecules and neutrophil infiltration; decrease of BBB integrity and blood flow by acting on endothelial cells, all of which lead to worse outcomes. Furthermore, IL-1 increases astrocyte proliferation and activation, resulting in astrocyte hyperplasia, a common response to brain damage. IL-1 up regulates a vast number of genes in astrocytes that encode neurotoxic factors including MMPs, chemokine’s, pro-inflammatory cytokines like IL-6 and TNF, as well as survival-promoting mediators like NGF, according to numerous studies (nerve growth factor).

IL-1 also affects cerebrovascular endothelial cells, increasing the production of chemo attractant and adhesion molecules like CCL-2, ICAM-1 (Inter-Cellular Adhesion Molecule-1), and E-and P-selecting, as well as promoting the breakdown of the Blood- Brain Barrier (BBB), all of which are associated with leukocyte recruitment. IL-1 can operate directly on neurons via an alternate signaling pathway involving ceramide formation and activation of Src kinase, which phosphorylates the NMDAR subunit 2B, resulting in greater calcium entry and increased sensitivity to further damage. Indirect neurotoxicity may be caused by IL-1's impact on the vascular endothelium, which promotes the migration of leukocytes, particularly neutrophils, which cause damage to the neurovascular unit by releasing MMPs and Reactive Oxygen Species (ROS).